It appears that nanobacteria and mycoplasmas may infect an individual in an
ongoing fashion for decades without actually directly threatening the life
of the individual. The progress of such infections appears to be aligned
with the progress of chronic diseases in general. It is, IMHO, logical to
attempt to correlate such infections with these diseases and look for
possible causal effect. This has been done for a number of chronic diseases.

I have been unable to find anything significant WRT research which makes any
serious attempt to link psoriasis and these chronic infections. I have found
a number of inferences, but no research.

Is anyone aware of any such research.

Did you read the crohns thread? And notice where
the study was done? Baylor. And where the p study
that started on DNA began? Baylor. Now if we could
get them to-gether some how. The learning curve for
all practical time purposes (not ours of course-as yesterday
is to late) is straight up and not published fast enough.
Peer review etc.

The NPF are the ones to ask as that DNA study is in house, now.
Go to www.npf.org (?) and get their 800#. Talk to as high
as you can get on the phone call. The higher you go, the more
they know. Hope full ly.

NOw, what if we (P) are a basket of maladies and a nanobac
infection is some how implicated. Heck, it could be
from conjunctivitis. Candida has 70+ endotoxins.
Strep, vaccines, etc etc etc

Now go back and read the post the other day on the
dairy council and scientific testing.

See what i mean. Testing for a few factors is hard
enough. How does one control for a myriad of
factors. (Well with out me, even with me.. it would
be hard if not impossibe)

Think of it this way. I speak or googlelate on the p ng.
You get it. (I dream on.)

YOU or some of youse p guys then:

Slurp some FSO. Or stop eating some flour. Or move
your vit. c far from the consumption of meat (high iron)
and quit your glass of wine before or with dinner (more
iron absorbtion). Iron in the intestines upregs P horrors.
Go on a high phyto chemical diet. (hint eat your five fruits+veggies)
And down tone the amount of PORK, EGGS (yolks) and
red meat by 10 to 75% per week, month, year. (hint-lower AA)
High arachidonics (AA) can even be generated from any old
omega 6 fatty acid with a little refined sugar to
click on the delta 5 desaturase to create cox 2’s (bad guys).
And remember omega 3 rich flax oil is
half and half omega 6. Why i limit to one tablespoon.
It may be essentail (EFA) and be half the problem.
While graham over there in england is two plus. (Tbls./day)
Of course he is in a colder clime then i and burns
it faster. (or he could hibernate in a heated house?)

Now, lets get down to nanobac or any bacteria or
pathogen. What if their role in this P condition is
sub-clinical? They or some of *them* bugs share
17% of our DNA. (This must frost the rear ends
of some religous extremists)

We are now enteron-ing the P twilight zone. A Rubics
cube in a pandorian box in a chinese box on a Rube
Goldberg contraption in a enigma… you get my drift.

In other words, we are it. The lucky 2.?% of the pop.
Once the bug is known (if it is a bug or his poop)
they (science folks) should be cruising down hill..
How else are we gonna arrive on a demographiccally
induced answer without talking and relating.
Only then, maybe, will a P-E-epiphany be possible.

And this is all for naught if its some simple
DNA glitch that causes the delta 5 saturase to
flip to fast and some PPAR (gamma, delta, alpha)
to be cytoclined to cascade some kinase to signal
some transduction in the what-it-ma-call-itz to
up or downregulate the th1/th2 imbalence that
throws the C-amp/C-gmp outa whack that makes
to much fibronectin that confuses the auto immune
and the antigens go haywire. Say, did i pull that
outa my rear or what? Time to go apoptosis.

PartII when my brain stops swimming in this swamp.

BACKGROUND: There is a growing interest in nonalcoholic
steatohepatitis (NASH), a disease entity which is quite similar to
alcoholic liver disease. MATERIAL AND METHODS: We present three
patients with nonalcoholic steatohepatitis, and review current opinion
on this disease entity. RESULTS: Non-alcoholic steatohepatitis is very
often associated with the insulin resistance syndrome. There is also
an association with hepatic iron overload. In one of our patients,
biochemical improvement occurred after treatment with phlebotomy.
Insulin resistance, resulting in fat accumulation, seems to be an
important first step in the pathogenesis. Free fatty acids, iron, and
other sources of oxidative stress probably result in cell damage. In
some patients, these events result in necroinflammation mediated by
various cytokines and immunoactive cells. The prognosis in pure
steatosis is usually good. Presence of necroinflammation or fibrosis
indicates a risk of progressive liver disease, including cirrhosis.